Oxidation of sodium sulphide by rat liver, lungs and kidney

Bartholomew, T. C.; Powell, Gavin; Dodgson, K. S.; Curtis, C. G.

doi:10.1016/0006-2952(80)90346-9

Cited by 110 publications

(68 citation statements)

References 18 publications

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“…Early indications of the metabolic lability of H 2 S came from labeling studies with [ 35 S]sulfide, which demonstrated its rapid oxidation by tissues with the efficiency being organspecific (26). Localization of sulfide oxidation activity to mitochondria was first reported more than two decades ago (27), and more recently, sulfide became the first inorganic substrate reported for human cells (28).…”

Section: Catabolism Of H 2 Smentioning

confidence: 99%

Redox Biochemistry of Hydrogen Sulfide

Kabil

Banerjee

2010

Journal of Biological Chemistry

679

526

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H 2 S, the most recently discovered gasotransmitter, might in fact be the evolutionary matriarch of this family, being both ancient and highly reduced. Disruption of ␥-cystathionase in mice leads to cardiovascular dysfunction and marked hypertension, suggesting a key role for this enzyme in H 2 S production in the vasculature. However, patients with inherited deficiency in ␥-cystathionase apparently do not present vascular pathology. A mitochondrial pathway disposes sulfide and couples it to oxidative phosphorylation while also exposing cytochrome c oxidase to this metabolic poison. This report focuses on the biochemistry of H 2 S biogenesis and clearance, on the molecular mechanisms of its action, and on its varied biological effects.Sulfur cycles through several biologically relevant oxidation states ranging from Ϫ2 as in hydrogen and metal sulfides to ϩ6 in sulfate. H 2 S, a colorless gas with the odor of rotten eggs, is important in the biogeochemical sulfur cycle and is used as an energy source by microbes such as the purple and green sulfur bacteria. It is a weak acid with pK a1 and pK a2 of 6.9 and Ͼ12 (1) and an aqueous solubility of ϳ80 mM at 37°C. Hence, at the physiological pH of 7.4, the ratio of HS Ϫ :H 2 S is 3:1. For brevity, H 2 S is used to refer to the total free sulfide pool (i.e. H 2 S ϩ HS Ϫ ϩ S 2Ϫ ) in this report unless noted otherwise. The ready ionization of H 2 S at physiological pH suggests impeded permeation through the lipid bilayer when compared with other gases, viz. NO or CO. On the other hand, transport of the gas, H 2 S, across the membrane does not appear to be facilitated (2).The toxicity of H 2 S is thought to have influenced evolution. The presence of a metastable H 2 S-enriched oceanic stratum is postulated to have limited early metazoan colonization of the continental shelf (3), and an increase in H 2 S has been implicated in the Permian-Triassic extinction Ͼ250 million years ago (4). However, the reputation of H 2 S as a toxic gas is enjoying a facelift, with increasing numbers of reports that it modulates a range of biological processes. Despite the rising interest in H 2 S biochemistry, fundamental questions regarding regulation of its production, its mechanism of action, and its destruction remain. In addition, perhaps most critical to the field is the issue of what constitutes biologically relevant levels of H 2 S with reports varying over a 10 5 -fold concentration range. Using a gas chromatography-based chemiluminescent sulfur detection method, free H 2 S (H 2 S ϩ HS Ϫ ) in blood was estimated to be ϳ100 pM, and in tissues, it was estimated to be ϳ15 nM (5). These values are considerably lower than the ϳ30 -300 M concentrations reported in a spate of recent studies (reviewed in Ref. 6). The high values can be ascribed to technical artifacts introduced by long processing times and harsh (either acidic or alkaline) conditions used to shift the equilibrium toward H 2 S or S 2Ϫ , respectively. Under these conditions, sulfide leaches from iron-sulfur cluster-containing p...

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Section: Catabolism Of H 2 Smentioning

confidence: 99%

Redox Biochemistry of Hydrogen Sulfide

Kabil

Banerjee

2010

Journal of Biological Chemistry

679

526

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“…1, time ϭ 0 h). Most of this 35 S 2Ϫ then disappeared, as it was incorporated into organic sulfur compounds, leaving approximately equal amounts in mutant and wild-type cells after 2 h. Over the next 20 h, wild-type cells gradually turned over this pool of 35 S 2Ϫ , but in the hmt2 Ϫ mutant this pool was not depleted. During that time, total (radioactive plus nonradioactive) sulfide levels accumulated more rapidly in the mutant than in wild type (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The 35 S-labeled glutathione peak diminishes in wild-type cells after two hours of cadmium exposure, while 35 Sphytochelatins rise steadily ( Figure 5B). In the mutant, glutathione levels decrease only slightly, while phytochelatins increase much more slowly than in the wild type.…”

Section: Phytochelatin Deficiency In the Hmt2 -Mutantmentioning

confidence: 99%

“…The growth of the hmt2 -mutant is not more sensitive than wild type to NiCl 2 (1-800 We also searched for oxidized phytochelatins using 35 S labeling. Extracts from radiolabeled hmt2 -cells were examined simultaneously by DTNB detection ( Figure 4A) and flow scintillation counting ( Figure 4B Figure 5A and 5B), which is consistent with previous assays.…”

Section: Phytochelatin Deficiency In the Hmt2 -Mutantmentioning

confidence: 99%

“…The slow rate of phytochelatin accumulation in the mutant could be consistent with either slower rates of phytochelatin synthesis, or normal rates of synthesis coupled with higher rates of degradation. If the latter explanation were true, we would expect a pulse of 35 S label to enter the phytochelatin pool at equal rates in the mutant and wild-type cells, but to "chase" out of the pool faster in the mutant than in wild type. In fact, the converse is true: 35 S-labeled phytochelatins appear more rapidly in the wild type cells than in the mutant, and levels in both strains remain elevated, with no evidence of differential degradation rates.…”

Section: Phytochelatin Deficiency In the Hmt2 -Mutantmentioning

confidence: 99%

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Molecular Genetics of Metal Detoxification: Prospects for Phytoremediation

Ow¹

2000

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Inorganic elements that include toxic metals and radionuclides present an unusual pollution challenge to ecosystems. These elements persist so that even low rates of deposition over time leads to toxic accumulation. Engineering nonfood plants to mine inorganics from contaminated sites offers an economically feasible solution for reclamation. Plants, however, generally have a low tolerance for these toxins. Oxidative stress is induced by high accumulation of heavy metals and radionuclides. Through a first strategy of analyzing fission yeast mutants, we identified and characterized several genes involved in heavy metal tolerance in the fission yeast. Most extensive characterization was conducted on a gene encoding a mitochondrial sulfide dehydrogenase. This gene prevents metal-induced sulfide toxicity in the mitochondria.Interestingly, highly homologous genes of unknown functions are also present in higher eukaryotes including humans.Through another strategy involving the direct expression and selection of cDNA clones in fission yeast, we identified approximately 50 cDNA clones that confer hypertolerance to cadmium and/or oxidative stress in fission yeast. These cDNAs have been sequenced and many of them have been transferred to vectors for transformation in plant and animal cells. By the end of the funding period, we were ready to test the function of these cDNAs when overexpressed in animal cells and transgenic plants.Functional identification of genes that ameliorate toxic effects of heavy metals and radionuclides will provide vital tools for engineering bioremediating plants.Additionally, these genes provide valuable insights into cellular defense mechanisms against exposure to these harmful oxidants.DOE final report -page 4 Research Objectives Introduction Promises of phytoextractionThe global industrial revolution has led to an unprecedented dissemination of toxic substances into the environment. Exposure to these pollutants, including dietary intake of plant-derived food and beverages, can have long-term effects on human health. This is of particular concern with substances that have a long biological half-life. The metal cadmium, for instance, can have a half-life of up to 30 years in the human kidney. Chronic bioaccumulation, at low quantities that might otherwise be considered insignificant, could nonetheless contribute to renal failure. Most organic compounds can be inactivated eventually through biotic and abiotic mineralization processes. Inorganic compounds, however, such as most heavy metals and some radionuclides, are practically indestructible. Their persistence in the environment requires that they be removed from the contaminated source or be converted into a biologically inert form. A conversion process is possible for only a few of the toxic elements, such as the biovolatilization of Se, Hg, and 3 H (2,38,50) . For most other toxic metals and radionuclides, effective remediation requires the physical extraction from soil and water systems. Conventional engineering technologies, the "dig and t...

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Sulfur reduction by human erythrocytes

1998

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Washed human erythrocytes incubated with glucose and S8 and purged with N2 produced H2S at a nearly constant rate of 170 μmol (L cells)–1 min–1, which continued for several hours. In sealed vials up to 25 mM HS– accumulated. Glucose caused the fastest H2S production, although either lactate or glycerol could support slower rates. When glucose was added without S8, anoxic H2S production nonetheless occurred at about 1.5% of the maximum rate, after 24 hr totaling 0.5 mmol H2S (L cells)–1, suggesting the presence of endogenous reducible sulfur. Anaerobic conditions were not required, since oxygenated cells produced H2S from S8 at 80% of the anoxic rate. Using cell lysates, production of H2S occurred after addition of either glutathione, NADH, or NADPH. The observations suggest possible physiological roles for H2S as an electron carrier, and are consistent with an evolutionary relationship between eukaryotic cytoplasm and sulfur‐reducing Archaea. J. Exp. Zool. 282:310–322, 1998. © 1998 Wiley‐Liss, Inc.

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Oxidation of sodium sulphide by rat liver, lungs and kidney

Cited by 110 publications

References 18 publications

Redox Biochemistry of Hydrogen Sulfide

Redox Biochemistry of Hydrogen Sulfide

Molecular Genetics of Metal Detoxification: Prospects for Phytoremediation

Sulfur reduction by human erythrocytes

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